华西口腔医学杂志 ›› 2012, Vol. 30 ›› Issue (6): 598-602.doi: 10.3969/j.issn.1000-1182.2012.06.009

• 基础研究 • 上一篇    下一篇

非受体型蛋白酪氨酸磷酸酶2与核因子-κB在糖尿病牙周炎牙周组织破坏中的作用研究

李昊1,2 李伟1 丁一1,3 郭斌4 谢红慧1,5 付敏1,5 王琪1,2   

  1. 1.口腔疾病研究国家重点实验室, 四川大学; 2.四川大学华西口腔医院修复科; 3.牙周科, 成都610041;4.中国人民解放军总医院口腔医学中心, 北京100853; 5.四川大学华西口腔医院老年口腔科, 成都610041
  • 收稿日期:2012-02-10 修回日期:2012-05-15 出版日期:2012-12-01 发布日期:2012-12-01
  • 通讯作者: 王琪,Tel:028-85503503
  • 作者简介:李昊(1984—),女,湖北人,住院医师,硕士
  • 基金资助:

    国家自然科学基金资助项目(81200794,81141062);四川大学青年科学研究基金资助项目(2010scu11099-4)

Affect of protein tyrosine phosphatase non-receptor type 2 and nuclear factor-κB on periodontal destruction with diabetes

Li Hao1,2, Li Wei1, Ding Yi1,3, Guo Bin4, Xie Honghui1,5, Fu Min1,5, Wang Qi1,2.   

  1. 1. State Key Laboratory of Oral Diseases, Sichuan University, Chengdu 610041, China; 2. Dept. of Prosthodontics, West China School of Stomatology, Sichuan University, Chengdu 610041, China; 3. Dept. of Periodontology, West China School of Stomatology, Sichuan University, Chengdu 610041, China; 4. Oral Medical Center, Chinese PLA General Hospital, Beijing 100853, China; 5. Dept. of Geriatric Dentistry, West China School of Stomatology, Sichuan University, Chengdu
    610041, China
  • Received:2012-02-10 Revised:2012-05-15 Online:2012-12-01 Published:2012-12-01

摘要:

目的观察糖尿病牙周炎条件下小鼠牙周组织中非受体型蛋白酪氨酸磷酸酶2(PTPN2)、核因子-κB(NF-κB)的表达与牙周组织破坏的关系。方法将4周龄健康雄性C57BL/6J小鼠随机分为正常对照组(N组)、单纯牙周炎组(P组)及糖尿病牙周炎组(DP组),每组6只。采用口内接种牙龈卟啉单胞菌法在P组建立牙周炎模型,采用腹腔注射链脲佐菌素结合高脂高糖食物与口内接种牙龈卟啉单胞菌法在DP组建立糖尿病牙周炎模型。各组动物于P、DP组末次细菌接种4周后处死,通过体视显微镜观察牙槽骨形态和附着丧失面积,采用苏木精-伊红(HE)染色法观察牙周附着丧失的高度,免疫组织化学法检测牙周组织中PTPN2与NF-κB的表达强度。结果P、DP组牙槽骨的附着丧失面积和牙周附着丧失高度均高于N组(P<0.05),PTPN2的表达量低于N组(P<0.05),而NF-κB的表达量则高于N组(P<0.01)。结论在糖尿病牙周炎的发生发展过程中,NF-κB可能有促进作用,而PTPN2可能有抑制作用;PTPN2的表达减少可能导致NF-κB表达增强而加重牙周组织破坏。

关键词: 糖尿病; 牙周炎; 非受体型蛋白酪氨酸磷酸酶2; 核因子-&kappa, B

Abstract:

Objective To investigate the expression of protein tyrosine phosphatase non-receptor type 2(PTPN2) and nuclear factor-κB(NF-κB), as well as the relationship between their expression and periodontal destruction in mice with diabetic periodontitis. Methods Four weeks old healthy C57BL/6J mice were randomly divided into normal control group(Group N), periodontitis group(Group P) and diabetic periodontitis group(Group DP), and each group
had six mice. Mice in Group P were inoculated Porphyromonas gingivalis orally to induce periodontitis. Mice in Group DP had high sugary and fatty food, streptozotocin intraperitoneal injection and Porphyromonas gingivalis oral inoculation to induce diabetic periodontitis. All mice were sacrificed 4 weeks after the last bacterium inoculation of Groups P and DP. Stereo microscope was chosen to detect morphological changes and bone loss areas of the alveolar bone. Hematoxylin-eosin(HE) staining was selected to observe loss heights of periodontal attachment. Immunohistochemical staining was used to detect PTPN2 and NF-κB expression in periodontal tissues. Results Group P and Group DP had significantly more attachment loss heights and areas than Group N(P<0.05), and showed less PTPN2 expression(P<0.05) and higher NF-κB levels(P<0.01). Conclusion PTPN2 may negatively regulate the development of diabetic periodontitis, while NF-κB may have opposite effects. PTPN2 down-regulation might contribute to NF-κB over -expression leading to exacerbated periodontal
destruction.

Key words:

diabetes; periodontitis; protein tyrosine
phosphatase non-receptor type 2; nuclear factor-&kappa,
B